An important class of mutagens acts by damaging DNA. For damage to be converted to mutation, new cellular processes must be expressed. In Escherichia coli, DNA damage induces expression of many new functions, including mutagenesis ("error-prone repair"). Since many processes are induced co-ordinately, understanding any one of them is proving difficult. The goal of the proposed research is therefore to understand in biochemical terms the mechanisms which control induction of all these new processes. Central to the induction process are the functions of two genes, recA and lexA. We intend to isolate transducing phages and hybrid plasmids carrying the lexA gene, and mutant alleles of that gene. We will identify the protein products made from the phage by infecting heavily UV-irradiated lysogenic cells, labeling the proteins made from the undamaged phage DNA, and resolving them by electrophoresis on SDA-polyacrylamide gels. We intend to identify among these proteins the product of the lexA gene, and to purify it. We will use the purified lexA product to test various models for its role in the induction process. Does it regulate gene expression, for example as a repressor? Does it interact with damaged DNA, or with ligands representing damaged DNA? Does it modify the functions of other proteins? We believe that understanding the biochemical role of the lexA protein is basic to further work in this field: It should help to dissect the error-prone pathway from other inducible processes; it may lead to discovery of similar regulatory processes in eukaryotic cells; it may provide the means for controlling induced mutagenesis; and it may uncover other cellular processes, also induced by mutagens and carcinogens, which prove to play a significant role in carcinogenesis.